Efficient rumen fermentation in ruminants is important to maximizing feed intake, feed efficiency, production of milk, meat, or other animal products, and maintaining acceptable levels of milk components. A healthy rumen environment reduces the risk and incidence of metabolic disorders that can occur with improper feeding management or abrupt feed intake changes, such as acidosis.
Current cattle industry practices incorporate the genetic selection of certain characteristics such as feed efficiency or maximized milk production. Genetic selection can result in animals that gain weight efficiently and/or produce large volumes of high quality milk. Genetically selected cattle are fed energy dense rations to maximize milk production. Energy dense rations can inhibit fiber fermentation and increase the difficulty of maintaining an optimal rumen environment. The feeding of high concentrate diets for cattle has increased awareness of problems associated with ruminal acidosis and the implications it has on feed consumption, feed efficiency, production of milk, meat, or other animal products, and animal health.
Current practices also include self-feeding for certain animals, which may include finishing beef and finishing dairy beef cattle. Self-fed nutrition management programs provide all or part of an animal's complete diet in feeder equipment that allows free access for the animal to this diet at all times of the day over the entire feeding period. Self-feeding often occurs in dry lot environments, but can occur in other environments as well. Typically, self-fed programs are designed for feeding beef and dairy cattle to the appropriate weight and fatness level whereby the resulting meat satisfies the standards of the meat industry. Self-fed programs can also be provided at any time during the growing and development periods for animals to achieve their desired weight and maturity. Because animals lack the nutritional wisdom to regulate their feed consumption to optimize health, growth, and beneficial rumen microbial growth, acute and subacute digestive disorders can result in these self-fed environments.
A substantial drop in ruminal pH can damage the rumen wall, decrease blood pH, cause dehydration, laminitis, or erratic feed consumption patterns, and severely depress feed intake and feed efficiency. During acidosis and the recovery period, females may also experience decreased milk production. Maintaining a healthy rumen pH and preventing disorders such as acidosis can therefore improve feed intake, feed efficiency, productive milk output, milk quality indices, and feedlot animal performance, including meat production.
One form of acidosis, subacute ruminal acidosis (SARA), is likely the most economically important disorder of dairy cattle in the United States. Economic losses due to SARA result from decreased feed intake, erratic feed consumption, decreased feed efficiencies, decreased milk production, decreased efficiency of milk production, premature culling, reduced animal health, and increased death loss. Severely affected herds commonly encounter extreme financial difficulties and often are forced to exit the beef or dairy industries.
SARA is defined as periods of moderately depressed ruminal pH (about 5.0 to 5.5) that are between acute and chronic in duration. The most consistent and immediate clinical sign of SARA is depressed feed intake. This is a normal, physiological effort by the animal to restore its ruminal pH to 5.5 or greater by reducing the supply of carbohydrates available for fermentation in the rumen. Fibrolytic bacteria are inhibited during periods of depressed ruminal pH, which decreases digestive efficiency. These factors combine to reduce such vital production variables as feed efficiency, milk yield, profitability, and impair animal comfort and health.
Health problems due to SARA may follow an initial drop in feed intake, weight gain, milk production and milk production efficiency. Clinical signs from SARA are delayed in onset from the time of the low ruminal pH insult. These signs are the result of a pathophysiological cascade of events that begins with rumenitis. Once the ruminal epithelium is inflamed, bacteria may colonize the papillae and leak into portal circulation. These bacteria may cause liver abscesses, which sometimes cause peritonitis around the site of the abscess. If the ruminal bacteria clear the liver (or if bacteria from liver infections are released into circulation), they may colonize in the lungs, heart valves, kidneys, or joints. The resulting pneumonia, endocarditis, pyelonephritis, and arthritis are all chronic inflammatory diseases that are difficult to diagnose ante-mortem. SARA may also be associated with laminitis and subsequent hoof overgrowth, sole abscesses, and sole ulcers. These foot problems generally do not appear until weeks or months after the bout of ruminal acidosis that caused them. Herds affected with SARA typically have high involuntary cull rates and high death losses.
Lactate accumulates transiently in the rumen of animals affected with SARA. This lactate is eventually absorbed as lactic acid or converted to less harmful organic acids. However, any lactate accumulation in ruminal fluid is undesirable because it has the potential to dramatically lower ruminal pH due to the very low pKa of lactate (3.9) compared to acetate, propionate, and butyrate (pKa of about 4.8).
Thus, there is a need in the art for a system and method for maintaining rumen health, including improving ruminal pH, in ruminants.